Mechanisms involved in the increased intestinal blood flow during glucose absorption appear to be predominantly dependent on metabolic circumstances or materials absorbed rather than neural or hormonal factors. Tissue PO2 is decreased one-third of normal in intestinal villi during absorption but tissue PO2 in the intestinal wall remains essentially normal. Previous studies do indicate that approximately 30% of the hyperemic response is related to oxygenation of the mucosal villi. Studies now in progress indicate that sodium ions absorbed with glucose diffuse from the villus to the intestinal wall and may increase intestinal wall tissue osmolarity by 60-70 mOsm. A change in osmolarity of this magnitude generally causes substantial vasodilation in the majority of vasculatures. Studies in the future will determine the sensitivity of the intestinal vasculature to various changes in tissue osmolarity. From such studies, the probable role of naturally occurring changes in tissue osmolarity during absorption in daily control of intestinal absorptive hyperemia can be deduced. Studies are also in progress to determine the extent of communication of vasodilation and vasoconstriction along arterioles and venules. This information is needed to evaluate whether or not arterioles in one area of the microvasculature can communicate their vasoactive status to other arterioles or different regions of the same arteriole. Both normal and spontaneously hypertensive rats are to be used in order to assess whether the hypertensive process enhances arteriolar communication and thereby augments neural and local vascular control.